DETERMINANTS OF VENTRICULAR PERFORMANCE

SHADAB KAMAL

INTRODUCTION

Human heart is functionally divided into right and left side. Each side may be further subdivided into a ventricle and an atrium.

The primary function of each atrium is to act as a reserviour and booster pump for venous return to the heart.

And , the primary physiological function of each ventricle is to maintain circulation of blood to the organs of the body .

The right ventricle receives blood from the systemic venous system and propels it through the lungs and onward to the left ventricle .

Whereas the left ventricle receives oxygenated blood from the pulmonary circulation and propels it through the systemic arterial network .

Although the ventricles are often thought of as functioning separately , their interdependence has clearly been demonstrated .

Moreover , factors affecting systolic and diastolic functions have been differentiated as:

Systolic functions mainly involves ventricular ejection , Whereas diastolic function is related to ventricular filling.

SYSTOLIC FUNCTION :

SYSTOLIC FUNCTION depends on CARDIAC OUTPUT

depends on

HEART RATE STROKE VOLUME

CARDIAC OUTPUT :

Ventricular systolic function is most often equated with cardiac output , which is defined as the volume of blood pumped by the heart per minute.

Because the two ventricles function in series, their outputs are normally equal . Cardiac output is expressed by the following equation :

CARDIAC OUTPUT = STROKE VOLUME X HEART RATE

To compensate for variations in body size , CO is often expressed in terms of total body surface area i.e.cardiac index.

Normal CI is 2.5 – 4.2 L/min/ m2. Because the normal CI has a wide range , it is relatively insensitive measurement of ventricular performance .

Abnormalities of CI therefore usually reflects gross ventricular impairment .

CI = CO / BSA

(1)HEART RATE :

Cardiac output is generally directly proportional to heart rate.

Heart rate is an intrinsic function of SA node but it is modified by autonomic , humoral, and local factors .

Enhanced vagal activity slows the heart rate via stimulation of M2 - cholinergic receptors , whereas enhanced sympathetic activity increases heart rate mainly through the activation of β1 - adrenergic receptors.

(2) STROKE VOLUME :

Stroke volume (SV) is the amount of blood ejected from the ventricle each time the ventricle contracts.

It is normally determined by :

(a) Preload

(b) Afterload

(c ) Contractility

(d) Wall motion abnormalities

(e) Valvular dysfunction

(a)Preload :

Ventricular preload is the end – diastolic volume , which is generally dependent on ventricular filling.

The relationship between cardiac output and ventricular end- diastolic volume is known as Starling’s law of the heart.

When HR is constant, CO is directly proportional to the preload, until excessive end diastolic volumes are reached .

At that point CO does not appreciably change or may even decrease. And over-distention of either ventricle can lead to excessive dilatation & incompetence of AV valves.

(b) Afterload :

Afterload refers to the resistance, impedance, or pressure that the ventricle must overcome to eject its blood volume .

It is determined by a number of factors, including the size and wall thickness of the ventricle, and the impedance of the vasculature.

In the clinical setting, the most sensitive measure of afterload is systemic vascular resistance (SVR) for the left ventricle and pulmonary vascular resistance (PVR) for the right ventricle..

Cardiac output is inversely related to afterload .

In patients with marked ventricular impairment it is very sensitive to acute increases in afterload.

(C) Contractility :

Cardiac contractility (inotropism) is the intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload .

It can be altered by neural, humoral, or pharmacological influences. Sympathetic nervous system activity normally has the most important effect on contractility.

Myocardial contractility is depressed by anoxia, acidosis, depletion of catecholamine stores within the heart, and loss of functioning muscle mass as a result of ischemia or infarction.

Most anesthetics and antiarrhythmic agents are negative inotropes (ie, they decrease contractility ) .

(d) Wall motion abnormalities :

Regional wall motion abnormalities may be due to ischemia, scarring, hypertrophy, or altered conduction.

Although contractility may be normal or even enhanced in some areas, abnormalities in other areas of the ventricle can impair emptying and reduce stroke volume.

(e) Valvular Dysfunction :

Valvular dysfunction can involve any one of the four valves in the heart and can lead to stenosis, regurgitation (incompetence), or both.

Stenosis of an AV (tricuspid or mitral) valve reduces stroke volume primarily by decreasing ventricular preload, whereas stenosis of a semilunar (pulmonary or aortic) valve reduces stroke volume primarily by increasing ventricular afterload .

In contrast, valvular regurgitation can reduce stroke volume without changes in preload, afterload, or contractility.

DIASTOLIC FUNCTION :

Ventricular diastolic function is related mainly to :

A. Ventricular Filling &

B. Cardiac Compliance .

(A) Ventricular Filling:

DETERMINANTS OF VENTRICULAR FILLING ARE : Venous return Blood volume Posture Intrathoracic pressure Pericardial pressure Venous tone Heart rate Rhythm (atrial contraction)

Venous return is the most important factor determining ventricular filling.

Changes in blood volume and venous tone are other important causes of intraoperative and postoperative changes in ventricular filling and cardiac output .

Any factor that alters the normally small venous pressure gradient favoring blood return to the heart like changes in intrathoracic pressure (positive-pressure ventilation ), posture (positioning during surgery), and pericardial pressure also affects cardiac filling.

Apart from these heart rate and rhythm can also affect ventricular preload, as increase in heart rate is associated with proportionately greater reductions in diastole than systole.

Absent (atrial fibrillation), ineffective (atrial flutter), or altered timing of atrial contraction (low atrial or junctional rhythms) can also reduce ventricular filling by 20–30%.

(B) Cardiac Compliance:

Technically compliance means change in volume for a given change in pressure .

Ventricular compliance is normally nonlinear .

With normal compliance, large increases in volume leads to a relatively small increases in pressure.

Whereas in a less-compliant ventricle, a greater pressure is generated with very little increase in volume.

Many factors are known to influence ventricular diastolic function and compliance.

Nonetheless, measurement of LVEDP or other pressures approximating LVEDP (such as pulmonary capillary wedge pressure) remains the most common means of estimating left ventricular preload .

Central venous pressure can be used as an index of both right as well as left ventricular preload in most normal individuals.

 

ASSESMENT OF VENTRICULAR FUNCTION

(a) Assessment of Systolic Function:

The ventricular ejection fraction (EF), i.e. the fraction of the end-diastolic ventricular volume ejected, is the most commonly used clinical measurement of systolic function.

EF can be calculated by the following equation:

Where EDV is left ventricular end diastolic volume and ESV is end-systolic volume.

EF = (EDV – ESV) /EDV

Normal EF is approximately 0.67 ± 0.08

Measurements can be made preoperatively from :-a) Cardiac Catheterizationb) Radionucleotide Studiesc) Transthoracic or TEE.

(b)Assessment of Diastolic Function:

Left ventricular diastolic function can be assessed clinically by Doppler echocardiography on a transthoracic or transesophageal examination.

Flow velocities are measured across the mitral valve during diastole.

ANAESTHETIC CONSIDERATION

EFFECT OF MECHANICAL VENTILATION ON VENTRICULAR PERFORMANCE

Mechanical Ventilation(MV) is associated with an inspiratory fall in aortic flow and systolic blood pressure .

Proposed mechanisms for the blood pressure fall with MV include: 1) reduced LV preload, 2) reduced RV preload, 3) increased PVR( pulmonary vascular resistance )

and RV impedance, and

With the commencement of MV , increase in airway pressure are transmitted to the intrapleural space & to the great vessels and other structures in the thorax .

As the airway pressure rises, the intrapleural pressure also rises & intrathoracic blood vessels become compressed causing the central venous pressure to increase .

This in turn , reduces venous return to the rt. heart & thus the rt. ventricular filling (preload ) volume. As a result, Rt. ventricular stroke volume decreases.

Positive airway pressure (Paw) is also transmitted to the pulmonary vasculature inducing a (small) rise in pulmonary artery pressure (Ppa) and RV impedance (afterload).

Left ventricular output may also be decreased when high tidal volumes are used during PPV , because the heart is compressed b/w the expanding lungs (i.e. Cardiac tamponade effect).

Mechanical or extrinsic PEEP (PEEPe)

It is commonly used to recruit alveoli and improve oxygenation during MV , further increases mean airway pressure during PPV , as reductions in venous return and cardiac output are greater during PPV with PEEP than PPV alone .

“So adequate pre loading should be done in COPD patient before starting mechanical ventilation as mechanical ventilation in these patient is associated with reduction in venous return thus the cardiac output as well”

Strategies to minimise these effects include:

1) the use of volume expansion to restore LV preload,

2) the use of assisted modes of ventilation to reduce increase in intrapleural pressure , and

3) the avoidance of high mean intra-thoracic pressure (Ppl) that may occur with a high minute volume, or PEEPe.

EFFECT OF INHALATIONAL ANAESTHETIC ON VENTRICULAR PERFORMANCE

NITROUS OXIDE :

Even though nitrous oxide directly depresses myocardial contractility in vitro, arterial blood pressure, cardiac output, and heart rate are essentially unchanged or slightly elevated in vivo because of its stimulation of catecholamines .

HALOTHANE :

It causes a dose-dependent reduction of arterial blood pressure due to direct myocardial depression.

ISOFLURANE :

Isoflurane causes minimal cardiac depression in vivo.

Cardiac output is maintained by a rise in heart rate due to partial preservation of carotid baroreflexes.

DESFLURANE

Its increasing dose is associated with a decline in systemic vascular resistance that leads to a fall in arterial blood pressure.

Cardiac output remains relatively unchanged or slightly depressed at 1-2 MAC .

Rapid increase in its conc. can lead to transient rise in H.R. , B.P. , & catecholamine levels.

EFFECT OF NEUROMUSCULAR BLOCKING AGENTS ON VENTRICULAR PERFORMANCE

SUCCINYLCHOLINE :

Low doses of succinylcholine can produce negative chronotropic and inotropic effects, but

higher doses usually increase heart rate and contractility and elevate circulating catecholamine levels .

Children are particularly susceptible to profound bradycardia following administration of succinylcholine

VECURONIUM :

Even at doses of 0.28 mg/kg, vecuronium is devoid of significant cardiovascular effects.

Potentiation of opioid-induced bradycardia may be observed in some patients.

ATRACURIUM :

Cardiovascular effects are unusual unless doses in excess of 0.5 mg/kg are administered.

However , it may cause a transient drop in systemic vascular resistance and an increase in cardiac index independent of any histamine release.

EFFECT OF INTRAVENOUS INDUCING AGENT ON VENTRICULAR PERFORMANCE

BARBITURATES :

Induction doses of intravenously administered barbiturates cause a fall in blood pressure and an elevation in heart rate.

It is frequently quoted that “more soldiers were killed in World War II by thiopental than by bullets.”So avoid induction with thiopentone in patient with shock

BENZODIAZIPINES :

The benzodiazepines display minimal cardiovascular depressant effects even at induction doses.

Arterial blood pressure, cardiac output, and peripheral vascular resistance usually decline slightly, whereas heart rate sometimes rises.

“So Midazolam is preferred as induction agent in patient with shock in low doses when ketamine and etomidate are not available” Comatose patients, those in severe shock, or in full arrest on admission, require nothing more than oxygen and possibly a neuromuscular blocking drug until the patient’s blood pressure and heart rate rebound enough that anesthetics can be added.

KETAMINE :

Ketamine increases arterial blood pressure, heart rate, and cardiac output . These indirect cardiovascular effects are due to central stimulation of the sympathetic nervous system and inhibition of the reuptake of norepinephrine

Accompanying these changes are increases in pulmonary artery pressure and myocardial work.

“In severe sepsis the catecholamine stores in body are depleted so induction with ketamine will lead to decompensated heart failure…so be cautious in patient with severe sepsis as direct action of ketamine on heart is myocardial depression”

PROPOFOL

The major cardiovascular effect of propofol is a decrease in arterial blood pressure due to a drop in systemic vascular resistance (inhibition of sympathetic vasoconstrictor activity), cardiac contractility, and preload.

ETOMIDATE

Etomidate has minimal effects on the

cardiovascular system. A mild reduction in peripheral vascular

resistance is responsible for a slight decline in arterial blood pressure.

Myocardial contractility and cardiac output are usually unchanged.

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